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Cardio Final > Valvular Heart Disease 1 > Flashcards

Valvular Heart Disease 1 Flashcards

1
Q

Right atrium and Right ventricle separated by

A

tricuspid valve

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2
Q

Right ventricle connected to pulmonary artery through

A

pulmonary semilunar valve

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3
Q

Left atrium connected to left ventricle by

A

mitral (bicuspid) valve

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4
Q

Left ventricle connected to aorta through

A

aortic semilunar valve

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5
Q

valves are part of the

A

endocardium

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6
Q

valves are covered by

A

endothelium

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7
Q

The interior of valves is composed of

A

dense connective tissue containing fibroblasts, collagen and elastic fibers, and extracellular matrix

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8
Q

How should valves look normally?

A

thin and nearly transparent

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9
Q

What valves are open in systole?

A

pulmonic valve and aortic valve

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10
Q

What valves are open in diastole?

A

mitral and tricuspid valve

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11
Q

Aortic valve normal anatomy

A

3 cusps

right coronary cusp
non-coronary cusp
left coronary cusp

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12
Q

Mitral valve normal anatomy

A

2 leaflets - anterior and posterior

2 papillary muscles (supply chordinae tendinae)

mitral valve orifice 4-6 cm^2

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13
Q

Mitral valve leaflets

A

Each leaflet divided in 3 segments

Anterior leaflet = A1, A2, A3

Posterior leaflet = P1, P2, P3

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14
Q

mark the joining of the leaflets

A

commisures

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15
Q

commissures in the mitral valve

A

anterior commissure

posterior commissure

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16
Q

what vascularizes the mitral valve

A

the coronary sinus and circumflex artery

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17
Q

right heart valves

A

tricuspid valve - 3 leaflets (anterior, posterior, septal)

pulmonic valve

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18
Q

Systole happens between (which heart sounds)

A

S1 and S2

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19
Q

On physical exam, the 4 auscultatory sites are

A

Aortic area
Pulmonic area
Tricuspid area
Mitral area

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20
Q

Intercostal space for aortic area on physical exam

A

btw. 2nd and 3rd intercostal

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21
Q

Intercostal space for pulmonic area on physical exam

A

btw. 2nd and 3rd intercostal

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22
Q

Intercostal space for tricuspid area on physical exam

A

btw. 4th and 5th intercostal

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23
Q

Intercostal space for mitral area on physical exam

A

btw. 4th and 5th intercostal

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24
Q

Normal findings on Physical exam

A

(1) Crisp S1 and S2
(2) Physiologic splitting of S2 (with inspiration, A2 then P2)
(2) No RV lift, PMI normal, JVP is 7cm H2O or less
(4) No diastolic murmur
(5) May have soft 2/6 “flow murmur” at left sternal border

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25
Q

On physical exam, hearing S3 may be normal in

A

children and young adults

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26
Q

Auscultatory findings (sounds)

A

Murmurs, Rubs, Clicks, Snaps

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27
Q

Murmur

A

turbulent flow (causes vibration)

in diastole or systole

can be from valvular disease or not
can be from stenosis or regurgitation

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28
Q

valvular stenosis

A

valve doesn’t fully open

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29
Q

valvular regurgitation

A

valve doesn’t fully close

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30
Q

Rub

A

scratchy, “squeaky leather” sound

from the rubbing of visceral and parietal pericardial layers

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31
Q

Systolic ejection click

A

high pitched sound of the aortic or pulmonic valve opening

occurs after S1 (systole)

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32
Q

systolic non-ejection click

A

high pitched sound of the closure of mitral valve

occurs after S1 (systole)

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33
Q

snap

A

short, high-frequency sound after S2 (diastole)

due to sudden arrest of the opening of mitral or tricuspid valve

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34
Q

mitral stenosis (MS) heard during

A

diastole

after S2

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35
Q

aortic regurgitation (AR) heard during

A

diastole

after S2

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36
Q

mitral regurgitation (MR) heard during

A

systole

after S1

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37
Q

aortic stenosis (AS) heard during

A

systole

after S1

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38
Q

Valvular Heart Diseases

A 
Bicuspid aortic valve
Mitral valve prolapse
Rheumatic valvular heart disease
Infective endocarditis
Calcific valvular disease
Nonbacterial thrombotic endocarditis
Carcinoid tumor
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39
Q

Other causes of valvular heart disease

A

Trauma
Syphilis
Ankylosing spondylisis
Marfan’s syndrome

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40
Q

Trauma (valvular heart disease)

A

ruptured papillary muscle

ruptured chordae

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41
Q

Syphilis (valvular heart disease)

A

Dilated aortic root; aortic insufficiency

Invasion of the Treponema pallidum into the ascending aorta through the lymphatics leading to the destruction of elastic and connective tissue

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42
Q

Ankylosing Spondylisis

A

Chronic inflammatory disease in men affecting the spine and sacroiliac joints

associated with HLA-B27

chronic inflammation leads to fibrosis and endarteritis of the aortic root

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43
Q

Marfan’s syndrome (valvular heart disease)

A

Aortic root dilation

Mitral valve prolapse

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44
Q

Bicuspid aortic valve etiology

A

congenital fusion of 2 of the 3 cusps during development

+/- calcification of cusps develops w age

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45
Q

Bicuspid aortic valve

A

most commonly due to fusion of LCC and RCC
affects 2% population
runs in families
+/- stenosis, +/- regurgitation

many patients go undetected and ever need repair or replacement

46
Q

Bicuspid aortic valve associated with

A

coarction of the aorta
Turner syndrome (45, X)
dilation of the ascending aorta

47
Q

In bicuspid aortic valve, more likely to have

A

dilated ascending > descending aorta

more likely to rupture
need aortic aneurysm screening w CTA or MRA
repair ascending aorta at 5cm (or 4.5 cm if having another surgery)

48
Q

Mitral valve prolapse (MVP) epidemiology

A

2%

males > females

49
Q

MVP etiology

A

genetic (AD)

associated with Connective Tissue diseases (e.g. Marfan’s)

50
Q

MVP histopathology

A

Valve collagen + elastic fibers fragment
Myxomatous Connective Tissue accumulates

–> weakened leaflets stretch

–> prolapse/balloon into left atrium in systole

51
Q

MVP associated with

A

infective endocarditis, palpitations, arrhythmias

52
Q

MVP causes

A

mitral regurgitation

degree of regurgitation determines if surgery warranted

53
Q

in MVP, the valve is repaired or replaced?

A

repaired

54
Q

what is controversial about MVP?

A

controversial recommendation to take antibiotics propr to invasive procedures to help protect against infective endocarditis

(most recent guidelines say not indicated; most cardiologists still do it)

55
Q

Rheumatic Heart Disease (RHD) epidemiology

A

children > adults

uncommon in industrialized countries; common in developing countries

56
Q

most common form of valvular heart disease worldwide

A

RHD (rheumatic heart disease)

57
Q

RHD etiology

A

group A beta-hemolytic streptococcus (GAS)

58
Q

RHD disease progression

A

3% strep pharyngitis infections —(2-3 wks)–> Acute Rheumatic Fever (ARF)

can lead to chronic RHD (result of endocarditis/valvulitis)

59
Q

Acute Rheumatic Fever results in

A

Pancarditis:

  • Endocarditis/Valvulitis (can lead to Chronic RHD)
  • Myocarditis (resolves)
  • Pericarditis (resolves)
60
Q

ARF diagnosis made by

A

Jones Criteria (5-15 years old)

need evidence of GAS infection and:
2 major or
1 major and 2 minor criteria

61
Q

Major criteria for ARF diagnosis

A

JNES

Joint - migratory polyarthritis (carditis) 
Nodules in skin (subcutaneous) 
Erythema mardinatum (skin rash w advanced edging and clearing center) 
Sydneham chorea (involuntary movements)
62
Q

Minor criteria for ARF diagnosis

A

MFIR

Migratory arythralgias
Fever
Increased acute phase reactants (ESR, CRP, leukocytosis)
PRolonged PR interval on ECG

63
Q

Evidence of streptococcal infection for diagnosis of ARF

A 
antistreptolysin 0 (AS0) antibodies
Positive throat culture for GAS
64
Q

RHD pathogenesis theory

A

GAS bacteria infect pharynx, skin, etc.

Antibodies develop to GAS M protein

Antibodies cross-react with heart tissues (type 2 autoimmune response)

Antibodies attack endocardium (valves, mitral > aortic > others), myocardium and pericardium

65
Q

Valves in ARF

A

valves swollen, inflamed

+ small fibrin vegetations at edges

66
Q

Myocardium in ARF

A

granulomas = Aschoff body

Macrophages in granulomas = Anischkow cells (with owl eye/caterpillar nuclei)

Degenerated collagen

67
Q

Chronic RHD pathogenesis

A

repair with fibrosis

68
Q

Chronic RHD valves

A

thickened with fibrosis
+/- fusion of neighbor leaflets/cusps

–> stiff valve

69
Q

Chronic RHD - which valve affected?

A

mitral > aortic > others

70
Q

Chronic RHD - chordae tendineae

A

thickened, shortened w fibrosis

71
Q

Chronic RHD - how long to develop?

A

10-30 years

72
Q

stenotic aortic valve with cup fusion

A

chronic RHD

73
Q

cusp fusion; thickened, fibrotic mitral valve and chordae tendineae

A

chronic RHD

74
Q

thickened, fibrotic, stenotic mitral valve lumen with leaflet fusion

A

chronic RHD

75
Q

Infective endocarditis (IE) definition

A

infection of endocardium of heart, specifically the valves

76
Q

IE etiology

A

bacteria&raquo_space; others

77
Q

IE - which valves affected?

A

mitral, aortic > others

78
Q

IE - 2 types

A

Acute bacterial endocarditis

Subacute bacterial endocarditis (SBE)

79
Q

Acute bacterial endocarditis

A

presents as an acute, fulminant infection

80
Q

SBE

A

presents with a more insidious course

81
Q

Acute Bacterial Endocarditis etiology

A

virulent organisms (e.g. staphylococcus aureus)

82
Q

Acute Bacterial Endocarditis dx progression

A

normal heart valve
rapid progression
valve damage/necrosis

83
Q

Acute Bacterial Endocarditis seen in

A

IV drug abusers
-when inject drug, innoculare with skin flora (Staph)
tricuspid valve (right heart) involved

84
Q

SBE etiology

A

less virulent organisms (e.g. streptococci viridans)

85
Q

SBE dx progression

A

abnormal heart valve (congenital, RHD, prosthetic)
insidious course
valve damage/necrosis LESS LIKELY

86
Q

Acute and SBE pathogenesis

A

normal/abnormal valve injury

+/- injury

fibrin thrombus formation on valve (=vegetation)

transient bacteremia (detnal, OB, catheters, etc.)

bacteria adhere to and colonize fibrin thrombusa

acute inflammation

+/- necrosis of valve

87
Q

Complications in Acute/SBE from fibrin thrombus formation (vegetation) +/- bacteria

A

embolize (septic emboli or aseptic emboli) –>

CNS, kidneys, spleen, skin, etc. –>

Infarcts and/or abscesses and/or hemorrhages (splinter, petechiae)

88
Q

Acute/SBE complications

A

septic embolus in brain

splinter hemorrhage

splenic infarcts

petechiae in conjunctiva

89
Q

IE cardiac lesions that predispose to endocarditis

A

anything that denudes endothelium off the surface of the heart

90
Q

Characteristics of infecting organisms in IE

A

(1) have access to the bloodstream
(2) survive in the circulation
(3) adhere to the endocardium

91
Q

Typical organisms in IE

A
  • Staphylococci (S. aureus, Coag neg staph)
  • Streptococci (viridans, enterococci, S. bovis, etc.)
  • Culture Negative (HACEK)
92
Q

Culture negative organisms in IE

A

rare, gram -, part of OP flora

H - haemophilus
A - aggregatibacter
C - cardiobacterium 
E - eikenella
K - kingella
93
Q

IE treatment

A

Prolonged IV and Oral antibiotics

Surgery to remove vegetations, abscesses or replace damaged valves

94
Q

IE prevention

A

oral antibiotics given BEFORE procedures likely to produce bacteremia

in patients with conditions that predispose to IE

95
Q

Calcific Valvular Disease (CVD) epidemiology

A

elderly (60s and 70s)

96
Q

most common cause of acquired valvular disease in the developed world

A

CVD

97
Q

CVD affects which valves?

A

left sided valves

98
Q

CVD pathogenesis

A

develop due to wear and tear on valve

inflammation similar to pathogenesis of atherosclerosis

active calcification by a “osteoblast-like” cell

can develop on congenital bicuspid valve

99
Q

CVD - valvue features

A

aortic/mitral valves with thickened, rigid, calcified cusps with calcified verrucae

100
Q

CVD - commissures

A

normal commissures

101
Q

CVD leads to

A

-aortic stenosis
(LVH and failure)

-mitral stenosis and regurgitation
(Pulmonary edema, pulm. HTN, A fib, HF)

102
Q

CVD - treatment

A

valve replacement (only effective treatment)

103
Q

Nonbacterial thrombotic endocarditis (NBTE) also known as

A

Marantic endocaditis

104
Q

NBTE epidemiology

A

occurs in patients with “wasting diseases”

i.e. cancer, adenoCA, blood; DIC, etc.

105
Q

NBTE pathogenesis

A

? increased coagulability or ? Ag-Ab

106
Q

NBTE - valve features

A

sterile fibrin vegetations

mitral and aortic valves

107
Q

NBTE affects which valves

A

left sided valves

mitral and aortic valves

108
Q

NBTE - complications

A

+/- embolize –> infarcts

109
Q

Carcinoid tumor definition

A

malignancy of neuroendocrine cells (lung, GI tract) that produce abnormally high levels of serotonin

110
Q

Carcinoid Tumor dx progression

A

serotonin induces fibrosis of the valvular endocardium of the right-sided valves –>

fibrosis causes thickening and restriction of the leaflets of the tricuspid and pulmonic valve –>

typically, leads to severe tricuspid regurgitation and severe pulmonic stenosis

111
Q

Carcinoid tumor -which valves affected?

A

right-sided valves

Cardio Final (6 decks)

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